Urushiol is the toxin responsible for the dermatitis caused by contact with the sap of commonly encountered noxious plants such as poison ivy (T. rydbergii (Northern and Western poison ivy) and T. radicans ssp. radicans (Eastern poison ivy)), poison oak (T. toxicarium (Eastern poison oak) and T. diversilobum (Western poison oak)), poison sumac (T. vernix), and related plants found throughout the world. These plants are in the Anacardiaceae group, which also includes, among others, the lacquer tree of Asia, the mango tree, cashew shell oil, and certain nutshells, such as the walnut. (Throughout this document, reference to poison ivy is meant to also include other urushiol containing plants.)
When located inside an unruptured plant, urushiol is a light, colorless oil. When exposed to oxygen, urushiol easily oxidizes and, after polymerizing, turns a blackish color. The slightest contact or even breeze easily damages the leaves. Therefore, it is rare to find a plant that does not have at least some ruptured leaves. Most people believe that poison ivy infection can only result from contact with the leaves of the plant. This is not true. Urushiol is found not only in the leaves but also vines and stem and root systems. The urushiol in the root system and vines is pure and is ten to 100 times more potent than that found in leaves. Accordingly, contact with cut or broken vines, or root systems will almost always result in a reaction.
Experts estimate there are up to 55 million cases of urushiol-induced contact dermatitis annually in the United States. Roughly 85 percent of all people will develop an allergic reaction when adequately exposed to poison ivy. People who reach adulthood without becoming sensitive have only a 50 percent chance of developing an allergy to poison ivy. Sensitivity to poison ivy tends to decline after 72 years of age as the immune system is less reactive. Children under the age of 1 year do not typically react to urushiol as their immune systems are not yet fully developed.
The American Academy of Dermatology estimates that there are up to 50 million cases of urushiol induced contact dermatitis annually in the United States alone. No one is sure of the number of world wide annual exposures but some experts estimate that the number could be double that of the United States. Accordingly, urushiol induced contact dermatitis is a world wide problem.
Chemically, urushiols are mixtures of catechols with long, hydrophobic, carbon (alkyl) side chains at the three position of the catechol ring. For example, poison ivy contains predominantly 3-n-pentadececylcatechols (C-15) and poison oak contains predominantly 3-n-heptaecylcatechols (C-17).
Current theory suggests that the reaction to urushiol is a delayed cell-mediated immune response in which, upon first exposure, urushiol penetrates the stratified squamous epithelial cells and binds to the Langerhan cells, which, in turn, sensitize effector T-cells in the lymph system. Subsequent exposures to urushiol result in the release of cytokines and reaction by macrophages and cytotoxic T-Cells. The result of lytic enzyme and perforin release is destruction of the membrane-bound urushiol and surrounding skin cells, which presents as the commonly seen clinical picture.
Once urushiol touches the skin, it begins to penetrate in minutes. It is completely bound to the skin after eight hours (two to six hours according to some experts). The rash generally develops within two days. Redness and swelling occur, often followed by blisters and severe itching. In a few days, the blisters may become crusted and begin to scale. The rash generally peaks after five days, and starts to decline after about a week or 10 days. The rash takes two or more weeks to heal. In a severe case or in a systemic reaction, individuals will many times present with black spots in areas of heavy urushiol concentration. The black spots are polymerized urushiol in a pure form and need to be removed immediately. This “Black Spot” test (attributed to Guin) is good indicator of a severe reaction, localized or systemic, or is often seen in cases of poison oak (typically a more tenacious reaction than poison ivy).
The rash can affect almost any part of the body, especially where the skin is thin, such as on the face. A rash develops rarely on the soles of feet and palms of hands, where the skin is thicker. The rash does not spread, although it may seem to do so when it breaks out in new areas. This may happen because urushiol absorbs more slowly into skin that is thicker, such as on forearms, legs and the body's trunk. Urushiol can be transferred by fingernails or animal fur and can remain on clothing, shoes, and tools for up to five years in moist climates and nine years in dry climates. Scratching the rash does not spread the urushiol to other parts of the body, but it can prolong the discomfort and cause a secondary infection.
Solution has historically consisted of attempting to remove the oil as quickly after exposure as possible: applying rubbing alcohol, washing affected areas with water, and showering with soap and water. In many instances, however, people either fail to fully remove the toxin before it has bound to the skin or don't realize they have been exposed until after the rash appears.
Over-the-counter solutions are legion; a partial list of the most popular includes hydrocortisone creams and ointments, diphenhydramine gels, calamine lotion, and the proprietary product, Ivy Dry®*. Hydrocortisone, diphenhydramine, and calamine lotion are palliatives and offer only temporary relief from the itching associated with Toxicodendron contact dermatitis. They do nothing to remove urushiol from the skin. Likewise, Ivy Dry® provides essentially a cooling effect that is only temporary. It may, if used before the urushiol binds to the skin, remove some of the urushiol.
Attempts have been made to find both prophylactic solutions as well as post-exposure solutions. To date, no vaccine has been developed and the prior art solutions are not without shortcomings. One solution example is seen in U.S. Pat. No. 5,686,074 to Stewart which teaches and claims a solution for poison ivy which includes a composition including linseed oil, an astringent, a starch, an essential oil and a citrus oil. One shortcoming of this patent is that linseed oil can cause irritation itself. A second shortcoming of this patent is that it requires that the composition be applied to the affected areas up to twice a day until the rash is gone. The composition provides what appears to be only very temporary palliative relief of poison ivy symptoms and does not appear to alter the course of the malady.
Other proposed solutions are seen in U.S. Pat. Nos. 5,620,527, 5,011,689 4,499,086, 4,259,318, 4,002,737, 3,862,331, 3,875,301, and 3,922,342.
Yet other prior art attempts have focused on prophylactics for preventing the dermatitis. One example is seen is U.S. Pat. No. 4,663,151 to Waali that discloses and claims a prophylactic solution based upon Aluminum Chlorhydrate.
Of course, the most significant shortcoming associated with prophylactic solutions is that they are only effective if applied before exposure to the urushiol; an occurrence that rarely takes place.
Tec Laboratories, Inc. of Albany, Oreg. markets an unpatented product sold under the mark Tech-Nu. This product also is not without shortcomings. This product was originally developed as a solution for radiation exposure. It was discovered, however, that the product also provided some relief for poison ivy exposure. The main active ingredient in the Tech-Nu® product is Octylphenoxy-polyethoxyethanol. The four octyl groups of this chemical are too large too surround the non polar moieties in the urushiol. Therefore, it only partially matches the polarity of urushiol. Thus, the action of this product renders the urushiol only partially inactive. Since the urushiol remains partially active and continues to cause irritation, only temporary relief is provided and multiple applications are necessary. Also, the chemical makeup of the product requires that it be applied no later than eight hours after exposure to urushiol.
There is need, therefore, for a safe, effective solution for dermatitis caused by exposure to the toxin urushiol. The solution should provide complete relief from the signs and symptoms associated with the dermatitis in limited solutions and be effective at any point during the dermatitis cycle.